Another example is FOXD1-AS1, which accelerates the processes of tumor growth, metastasis, and chemoresistance on in vitro and in vivo GC models through two mechanisms: (1) its effects on miR-466 function (explained later) and (2) the fact that FOXD1-AS1 is able to promote the phosphorylation of 4E-BP1, and thereby, provokes the activation of eIF4E (p-eIF4E), which facilitates the translation of FOXD1 that finally is the one that will trigger these malignant features [80]. The gene discussed is EIF4E; the disease is neoplasm.